Spontaneous Breathing Improves Lung Aeration in Oleic Acid–induced Lung Injury

Wrigge, Hermann; Zinserling, Jörg; Neumann, Peter; Defosse, Jérôme; Magnusson, Anders; Putensen, Christian; Hedenstierna, Göran

doi:10.1097/00000542-200308000-00019

Cited by 167 publications

(129 citation statements)

References 33 publications

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“…We could not completely exclude a possible influence of the instrumental apparatus used for the pneumoperitoneum induction on hemodynamics. Nevertheless, its impact on the edema formation, if any, is questionable because the excess tissue mass recorded under these conditions was similar or even smaller than previously reported (29,31).…”

Section: Oleic Acid-injured Lungsupporting

confidence: 43%

“…Although the rise in Ppa has been already described in different experimental settings (27)(28)(29), the increase in mean arterial and occlusion pressures has not been previously reported (30). We could not completely exclude a possible influence of the instrumental apparatus used for the pneumoperitoneum induction on hemodynamics.…”

Section: Oleic Acid-injured Lungmentioning

confidence: 72%

See 1 more Smart Citation

An Increase of Abdominal Pressure Increases Pulmonary Edema in Oleic Acid–induced Lung Injury

Quintel

Pelosi

Caironi

et al. 2004

Am J Respir Crit Care Med

169

108

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Increased abdominal pressure is common in intensive care unit patients. To investigate its impact on respiration and hemodynamics we applied intraabdominal pressure (aIAP) of 0 and 20 cm H 2 O (pneumoperitoneum) in seven pigs. The whole-lung computed tomography scan and a complete set of respiratory and hemodynamics variables were recorded both in healthy lung and after oleic acid (OA) injury. In healthy lung, aIAP 20 cm H 2 O significantly lowered the gas content, leaving the tissue content unchanged. In OAinjured lung at aIAP 0 cm H 2 O, the gas content significantly decreased compared with healthy lung. The excess tissue mass (edema) amounted to 30 Ϯ 24% of the original tissue weight (455 Ϯ 80 g). The edema was primarily distributed in the base regions and was not gravity dependent. Heart volume, central venous, pulmonary artery, wedge, and systemic arterial pressures significantly increased. At aIAP 20 cm H 2 O in OA-injured lung, the central venous and pulmonary artery pressures further increased. The gas content further decreased, and the excess tissue mass rose up to 103 Ϯ 37% (tissue weight 905 Ϯ 134 g), with homogeneous distribution along the cephalocaudal and sternovertebral axis. We conclude that in OAinjured lung, the increase of IAP increases the amount of edema.Keywords: intraabdominal pressure; acute respiratory distress syndrome; pulmonary edema; lung mechanics; computed tomography scanThe importance of intraabdominal pressure (IAP) in acute lung injury and acute respiratory distress syndrome has been recently suggested (1). For a long time any change in respiratory mechanics in patients with acute lung injury/acute respiratory distress syndrome was attributed to lung mechanics, whereas chest wall mechanics was assumed to be normal. However, few studies in which chest wall elastance was actually measured have showed that it was abnormal in a substantial proportion of patients with acute lung injury/acute respiratory distress syndrome (2-4). We (5) and others (6) have described different chest wall mechanics in patients with pulmonary and extrapulmonary acute respiratory distress syndrome, mainly due to different IAP values.However, apart from respiratory mechanics, the increased intrathoracic pressure caused by chest wall impairment may have important consequences on hemodynamics (7). We investigated the effect of changing IAP during controlled mechanical ventilation in healthy and diseased lungs. Surprisingly, the increase of IAP had an unexpected impact on lung edema, likely related to its formation and clearance. We wish to report our findings and METHODS(Additional details about Methods are provided in an online supplement.)The study group consisted of seven anesthetized and paralyzed domestic pigs (41 Ϯ 4 kg) ventilated throughout the experiment in supine position, with a Vt of 12 ml/kg, respiratory rate of 12-14 breaths/minute, positive end-expiratory pressure of 5 cm H 2 O, and Fi O 2 of 1.0. The animals were fully instrumented for hemodynamic monitoring (carotid artery, right atrium, mea...

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Section: Oleic Acid-injured Lungsupporting

confidence: 43%

Section: Oleic Acid-injured Lungmentioning

confidence: 72%

An Increase of Abdominal Pressure Increases Pulmonary Edema in Oleic Acid–induced Lung Injury

Quintel

Pelosi

Caironi

et al. 2004

Am J Respir Crit Care Med

169

108

View full text Add to dashboard Cite

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“…As described above, the APRV methodologies were subdivided into two categories: F-APRV; (Tables 1 and 3) and P-APRV (Tables 2 and 4). The majority of the animal studies (69 % of total) [2,4,[7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26] and human studies (82 % of total) [3, were in the F-APRV category.…”

Section: Methodsmentioning

confidence: 99%

“…Many crossover trials showed similar or increased oxygenation with lower peak pressures and no negative effect on hemodynamics with APRV as compared with CPPV [2,3,17,[27][28][29][30][31][32][39][40][41][42], and some studies showed hemodynamic improvement with APRV [13,24,36,39]. Prospective randomized trials comparing APRV and CPPV showed that APRV is safe and potentially beneficial (Table 3).…”

Section: Outcomementioning

confidence: 99%

Experiences Using Airway Pressure Release Ventilation for Pneumonia with Severe Hypercapnia or Postoperative Pulmonary Edema

Hong

Lee

2017

Korean J Crit Care Med

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Airway pressure release ventilation (APRV) was first described in 1987 and defined as continuous positive airway pressure (CPAP) with a brief release while allowing the patient to spontaneously breathe throughout the respiratory cycle. The current understanding of the optimal strategy to minimize ventilator-induced lung injury is to "open the lung and keep it open". APRV should be ideal for this strategy with the prolonged CPAP duration recruiting the lung and the minimal release duration preventing lung collapse. However, APRV is inconsistently defined with significant variation in the settings used in experimental studies and in clinical practice. The goal of this review was to analyze the published literature and determine APRV efficacy as a lung-protective strategy. We reviewed all original articles in which the authors stated that APRV was used. The primary analysis was to correlate APRV settings with physiologic and clinical outcomes. Results showed that there was tremendous variation in settings that were all defined as APRV, particularly CPAP and release phase duration and the parameters used to guide these settings. Thus, it was impossible to assess efficacy of a single strategy since almost none of the APRV settings were identical. Therefore, we divided all APRV studies divided into two basic categories: (1) fixed-setting APRV (F-APRV) in which the release phase is set and left constant; and (2) personalized-APRV (P-APRV) in which the release phase is set based on changes in lung mechanics using the slope of the expiratory flow curve. Results showed that in no study was there a statistically significant worse outcome with APRV, regardless of the settings (F-ARPV or P-APRV). Multiple studies demonstrated that P-APRV stabilizes alveoli and reduces the incidence of acute respiratory distress syndrome (ARDS) in clinically relevant animal models and in trauma patients. In conclusion, over the 30 years since the mode's inception there have been no strict criteria in defining a mechanical breath as being APRV. P-APRV has shown great promise as a highly lung-protective ventilation strategy.

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“…The study demonstrated that increases in tidal volume with positive-pressure ventilation failed to alter V D /V T , suggesting greater dead space from overdistention of al- Experiments in a porcine model have further defined the advantages of spontaneous breathing in enhancing ventilation perfusion relationships and oxygenation. 56,57 Using both computed tomography and a ␥ camera technique, one group demonstrated that lung injury with oleic acid resulted in a predictable fall in end-expiratory lung volume and oxygenation. Animals were either maintained on controlled ventilation or allowed to breathe up to 30% of the total minute volume spontaneously.…”

Section: The Importance Of Spontaneous Breathingmentioning

confidence: 99%

Should Intermittent Mandatory Ventilation Be Abolished?

Kacmarek

Branson

2016

Respiratory Care

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Intermittent mandatory ventilation (IMV) was introduced nearly 50 years ago. Despite the initial fanfare and early adoption by many, the role of IMV continues to be questioned. The use of small tidal volumes complicates the application of IMV, and issues with work of breathing, weaning and lack of clear advantages have many calling for a moratorium on its use. Spontaneous breathing, however, has a number of salutatory effects on gas exchange, the distribution of ventilation, and hemodynamics. These issues will be explored in light of a growing body of evidence. Key words: Mechanical ventilation, intermittent mandatory ventilation, synchronized intermittent mandatory ventilation, asynchrony and work of breathing. [Respir Care 2016;61(6):854 -866.

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Spontaneous Breathing Improves Lung Aeration in Oleic Acid–induced Lung Injury

Abstract: The results support the hypothesis that spontaneous breathing during APRV improves oxygenation mainly by recruitment of nonaerated lung and improved aeration of the lungs.

Cited by 167 publications

References 33 publications

An Increase of Abdominal Pressure Increases Pulmonary Edema in Oleic Acid–induced Lung Injury

An Increase of Abdominal Pressure Increases Pulmonary Edema in Oleic Acid–induced Lung Injury

Experiences Using Airway Pressure Release Ventilation for Pneumonia with Severe Hypercapnia or Postoperative Pulmonary Edema

Should Intermittent Mandatory Ventilation Be Abolished?

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